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 To Vitamin K or Not To K, That is the question w/Afib 
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Ascorbate Wizard
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Post To Vitamin K or Not To K, That is the question w/Afib
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I'm in total agreement with Owen that V-K can reduce blood vessel calcification. However the downside is this gentleman also has A-fib. As such V-K can promote clotting factors which with A-Fib can and will cause clots to form which could have some bad effects. Promoting the clotting factors would be counter productive at this point.


Thought the discussion of vitamin K and AFIB merited its own discussion. Ergo, rather than detract from the thread on supplements for reducing high blood pressure, here we go.

I have always wondered about this standard medical advice (to avoid vitamin K) given to heart patients. The late Mr. Till was advised not to eat salads for this very reason!! (Which made some sense, I supposed, since he was on coumadin.) So heart patients are told to avoid vitamin K, yet their intestinal flora, if healthy, is making vitamin K 24/7 !?

I don't think vitamin K "promotes" clotting factors any more than vitamin C "promotes" collagen. In other words, taking enormous amounts of vitamin C does not create large callouses of collagen under the skin! The body makes what it needs, and then uses ascorbate for other purposes. I believe it is the same with vitamin K. I don't know of any evidence that the more vitamin K one takes, the more the blood tends to clot without any reason.

Yes, vitamin K is required in a clotting pathway, such that if it is not present, the ability for blood to clot is diminished. The anti-clotting drugs, such as warfarin, coumadin, heparin, etc. work in different ways to interfere with vitamin K, and its role in the clotting process.

I began to understand why medicine uses these drugs after reading Dr. Levy's STOP AMERICA'S #1 KILLER. Some plaques are unstable and the risk of MI is high. His explanation of advanced, aged, unstable plaques reminds one of the growth of ordinary tissue. These plaques can develop their own set of capillaries. As Levy points out, capillaries are weak blood vessels, so when they grow near the heart, the blood pressures are high and risk of rupture increases. A rupture and the subsequent clotting cascade usually leads to an MI. These vitamin K antagonist drugs would thus serve a purpose in certain cases, i.e., to interfere with blood clotting caused by broken capillaries. So it is hard to argue with the use of these drugs in people with advanced plaques being fed by a system of capillaries. (But this risk has to be balanced against the possibility of bleeding in other areas, e.g. in the brain, or from an accident.)

Then there is the issue of calcification. (It is possible one reason rather weak veins keep bypass patients alive for decades is because the veins are being unintentionally strengthened as they become calcified) from the use of the blood thinners.

I suppose there is a balance, but we do know that either a low intake of vitamin K, or taking those vitamin K antagonist drugs will rapidly increase calcification. There is anecdotal evidence (and some clinical evidence) that the arteries will return to a more normal condition after vitamin K supplementation.

I guess I don't understand the clotting concern w/r to AFIB? (I don't know if the family has gotten a clear picture of what really happened, but they were told the Mr. Till had a collapsed blood vessel, perhaps one of his bypass graphs, limiting blood flow to the heart. We have to assume that this is at least one reason why the heart developed AFIB in his case.)


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Owen R. Fonorow, Orthomolecular Naturopath


Wed May 25, 2011 8:11 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
When a patient presents with A-fib and calcification a decission must be made, which is more lethal? At first thought, the A-fib must be of prime concern unless the calcification is impeding the blood flow. Generally they are isolated instances and a AFA (A-Fib Assement) will be preformed to determine the cause. Then the manner of treatment will be determined and the risks involved. Ie. If anti-coagulation drugs are introduced would it increase the amount of calcification and how much is tolerable before action must be taken. If the A-fib can be controlled by other meds then the calcification can be addressed. The point I'm trying to make is when there is a greater problem it must be addressed first. To adminster therapy to one problem that would be detrimental to a more serious problem wouldn't be good practice.

Vitamin-K does mobilize calcium and I'm in agreement it would be a good choice to remove vascular calcification provide there is no other problem.

Here's a link from the Linus Paulinin Institute.
http://lpi.oregonstate.edu/infocenter/v ... /vitaminK/

You'll also note this statement which I love, Because it finally shows the powers to be are finally getting their head out of their Butt and realizing the body needs some types of vitamins to live.

Quote:
Experts now advise a reasonably constant dietary intake of vitamin K that meets current dietary recommendations (90-120 mcg/day) for patients on vitamin K antagonists like warfarin



Owen on your last statement check out Neo-intimal hyperplasia might give you some clue as to what could have happened.

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Wed May 25, 2011 11:19 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Quote:
If anti-coagulation drugs are introduced would it increase the amount of calcification and how much is tolerable before action must be taken. I


I am trying to understand the reasoning. I infer that in your experience, the vitamin K antagonists are useful in treating A-FIB. I am trying to understand why?


Regarding http://en.wikipedia.org/wiki/Intimal_hyperplasia The connection I am trying to understand is why impeded blood flow leads to AFIB? Maybe the conditions were independent - the collapsed graph and the AFIB, but they were probably related, correct?


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Thu May 26, 2011 7:18 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
I'm a little short on time today so I'll have to answer each question seperately.

When A-fib is present the top chambers of the heart called the atrium goes into a spasm or quiver which is very ineffective in pumping blood. Normally it just contracts like squeezing the bulb of a BP cuff forcing the blood out of the chamber very effectively. With A-fib pools of blood sit in the chamber and as blood does when it's not in motion it begins to coagulate. When the A-fib passes and normal rythm returns these clots are sweep out of the atrium and into the circulatory system where they can become stuck and cause blockage. If they get stuck in the brain you have a stroke, in the heart a heart attack you name it it'll affect it. When anti-coagulation drugs are introduced your slowing the clotting time which means the blood can sit longer before it clots giving you more time to recover from the a-fib episode before you form clots in the chamber. Reducing your risk of adverse reactions. Yes these drugs have side effects but there easier to handle then a clot stuck in the brain.
Hope this clears this point up a little. Bottom line your buying time before bad happens.
I'll answer the other question later! :)

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Thu May 26, 2011 9:07 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
First of all some of my descriptions may elicit scary feelings, thoughts etc. my only intent is to exemplify a body reaction in a descriptive manner.

We’ve all I’m sure have seen so called Western Movie where a team of Horses is pulling a stage coach going across the plains creating a cloud of dust in it’s wake and moving right along. The Human heart works in the same manner a team of components operating in sequence and accomplishing a given task.
So our team of horses are all bridled together and performing as they should when all of a sudden one of the team Drops dead. Since he is tied to the rest of team. Chaos breaks loose horses that are healthy begin to trip and fall all over themselves hurting the other horse and the person who haves control over them has a handful trying to restore order well things are flying all over the place. The point here is if a part fails there will be reactions to the rest of the system.
The heart works the same way if there is a failure in the system order must be restored as it will effect other parts.
In basic anatomy we learn that arteries and veins are composed differently and each component of these vessels has a different function. Yet in modern medicine we strive to fool the body into thinking that using vein’s for arteries is ok. The vein is soaked in chemicals that allow the body to recognize it as it’s own and not try to dispose of it but the body is smart and after a period of time it begins making demands of the vein to act like an artery it’s being used for. The lining inside arteries is made up of cells called endothelial cells. There appearance is that of water lilies they have a stem and they overlap and press against each other. Arteries also have a muscle wrapped around them so they can expand and contracted as demands call for. The endothelial cells have to maintain a inner seal to prevent the blood they carry from leaking around them and maintain this seal wither constricted or expanded. Another and important function of the cells is they produce Nitric Oxide which keeps the muscles of the vessels in a relaxed state. The body monitors these levels and when there is more demand to meet the needs it will find ways to increase these’s levels. What can cause this fall in levels? Things like plaque build up over a bunch of Damaged Endo cells preventing release of NO into the stream. A section of blood vessel carrying blood out but not producing NO (CABG). Lets look at this from the view of the body. Here’s a vessel not producing NO but carrying Oxygen rich blood, “It needs endothelial cells in it to meet demands!!”
Let’s put some in there!!
Lets look at the point of grafting we have a vein stuck in an artery they have healed together on the outside and upon closer look they have bound to the muscle of the artery but there is no endothelial cells in this pipe. So the body sends the necessary components to start building cells there. Problem!!! Endothelial cells won’t grow in veins. They grow in arteries so the artery starts growing more and more at this point it begins to cover the opening of the graft and eventually close off this opening. OOPSS! Why was that vein here?? Back to square one Push it open and put a stent in it make sure it releases poison to kill those nasty endothelial cells. Ah!! Relief two or three years later the poison wears off but the body still wants more NO and it starts all over again. Now what??
In the mean time the reason the graft was put in there in the first place. Once again not receiving the oxygenated blood it needs, begins to necrotize (die)
And what does necrotized tissue do?? Nothing, it becomes what is known as Akinetic. Like the dead horse it prevents that part of the heart from doing it’s job properly. Since it can’t push the blood out properly it begins to back up into the upper chambers of the heart and they begin to stretch with the rise in pressure. Around the outer perimeter of the atrium and inside, are the nerves which control the beating of the heart as the tissue stretch’s these nerve’s start to separate and loose their connection resulting in dysynchrony and ultimately failure of the organ. Sad but it happens more often then told.
As always the question what can be done to prevent this from happening??
If you or yours has had bypass surgery where a vein was used. It’s a must to keep your Nitric Oxide levels up so the demand is quelled.
How L-Arginine and or L-citrulline.
It’s been 10 years since my Bypass! I ain’t had No trouble!!
Good !! The average found on this is Usually in the 1st to the 3Rd year =60% then 10th to the 15th year =35%. 5% Never. Great Odd’s Right!
Owen Hope this helps with your quest for understanding.

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Thu May 26, 2011 3:29 pm
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Remember there is no medicine to cure this and anything with a L- is just a supplement.
Here's a presentation from 1997 it go's into the medicalize of it so you can see till big pharma comes up with a money maker to do away with symptoms and keep people going till they empty their wallet. You have to look under the rug for a real fix.
Or take PT to prevent it in the first place!!!

http://www.ncbi.nlm.nih.gov/pmc/article ... 7-0010.pdf

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Thu May 26, 2011 8:21 pm
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Johnwen --
For me, L-Arginine fosters development of blisters/sores on my lips, even though I take 6 grams of L-Lysine each day. Is there something else that will promote nitric oxide production without this effect? Or is there a nitric oxide supplement that could be taken instead?
thanks so much...
Eve


Fri May 27, 2011 6:22 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
I would think, but I don't know for sure, that lysine would also promote NO as it like all amino acids, contains nitrogen, and I believe lysine is a nitrogen donor.

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Fri May 27, 2011 7:48 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Quote:
How L-Arginine and or L-citrulline.


Quote:
Arginine is first oxidized into N-hydroxyl-arginine, which is then further oxidized to citrulline concomitant with release of nitric oxide.



http://en.wikipedia.org/wiki/Citrulline

http://www.vitaminshoppe.com/search/en/ ... n=vitamins

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Fri May 27, 2011 8:32 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Quote:
This became evident when these receptors were blocked by arginine-uptake inhibitors such as L-lysine which functions as antagonist of these glutamate receptors.



http://www.whatislife.com/reader2/Metab ... ay/no.html

http://www.cindeegardner.com/boom2.htm


You'll find Supps that combine these two together as you can see it's a push pull war being created. If your going to take L-Arginine and L-Lysine seperate them by at least a couple of hours and take low dose amounts of Arginine. Like Proline your body make it's own but just needs a little help adding to the mix.
The links above are for educational purposes and not intended to endorse their products whatever their selling. :)

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Fri May 27, 2011 10:48 pm
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Quote:
When a patient presents with A-fib and calcification a decission must be made, which is more lethal? At first thought, the A-fib must be of prime concern unless the calcification is impeding the blood flow. Generally they are isolated instances and a AFA (A-Fib Assement) will be preformed to determine the cause. Then the manner of treatment will be determined and the risks involved. Ie. If anti-coagulation drugs are introduced would it increase the amount of calcification and how much is tolerable before action must be taken. If the A-fib can be controlled by other meds then the calcification can be addressed. The point I'm trying to make is when there is a greater problem it must be addressed first. To adminster therapy to one problem that would be detrimental to a more serious problem wouldn't be good practice.


Thanks to Owen and Jonwen.

I read everything that both of you wrote about a-fib and calcification

However, I find myself confused.

For someone like me who has a-fib and "some calcification" (see next paragraph), what is the bottom line? Is the only way for me to reverse my blockage (and reverse calcification) to take supplemental vitamin K ...OR... can I get the same effect by eating salads like I have been doing for a long time? (I have been thinning my blood naturally for 20 years with flaxseed oil and vitamin E and have had no problem). [my dad did the same thing and he had a-fib]

[PLEASE NOTE => I thought cardio's said I had calcification in an area away from the blockage...like at a particular juncture but not in the main blockages]

If the only way to get to totally get rid of calcification is vit K supplementation....then MAYBE I should consider being on blood thinner (which I hate the idea of).

Thanks again, Doug


Mon May 30, 2011 4:58 pm
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
I'll defer to johnwen - but you lost me at
Quote:
If the only way to get to totally get rid of calcification is vit K supplementation....then MAYBE I should consider being on blood thinner (which I hate the idea of).


Generally the "blood thinners" are vitamin K antagonists - really anti-clotting drugs. These drugs generally increase calcification in soft tissue - throughout the body. What I think I learned from Johnwen is that some (all?) people with A-FIB have pools of blood that are not expelled properly by the heart and thus can form clots. To me, the likelihood of this condition would dictate the treatment options.

Johnwen, perhaps an "anti-platelet" drug (even aspirin) along with vitamin E, enzymes, etc. would be as effective in controlling the potential clotting?

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Tue May 31, 2011 6:48 am
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Ascorbate Wizard
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Quote:
If the only way to get to totally get rid of calcification is vit K supplementation....then MAYBE I should consider being on blood thinner (which I hate the idea of).


Doug:
This is a call between you and your doc he knows more then anyone whats going on there and has the knowledge to make a call on which way to go. I'm sure he would make a judgement which would be the best approach. On this and other forums we can advise and tell you which supplements would be benefical. But when it comes to a matter of your safety He's the Man or Women! You should ask him his feelings on your situatiton and his long term ideas.

Quote:
Johnwen, perhaps an "anti-platelet" drug (even aspirin) along with vitamin E, enzymes, etc. would be as effective in controlling the potential clotting?


This is the Sledge hammer and the feather comparision! With A-fib the range considered proper is INR 2.0 to 3.0. Whats that mean? Ok when they draw blood and prepare it then they time how long it takes to coagulate. Normal ranges is called your Protrombien Time or PT. The time Range is 9.7 to 12.7 Seconds. Inr which is International normalized ratio is approx 11.08 Seconds so if your PT is normal you'll have @ 1 inr. +/- a decimal. To achive a 2.0 Inr the cloting time would have be 22.16 Seconds to get 3.0 - 33.24 seconds which is pretty thin. With asprin you would probably have comsume a bottle or better a day to achive these levels. Your tummy would be a complete mess after a few days if you survive that long. A few a day would bring up your pt but but not enough to reach what is classified as a Safe level. However if the A-fib is short and few it would be a Step in the right direction.

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Tue May 31, 2011 2:37 pm
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Vitamin C Master
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Post Re: To Vitamin K or Not To K, That is the question w/Afib
Vitamin K2 supplementation has been suggested as the proper treatment for artery calcification in patients on coumarin-derivatives (Warfarin, etc.):

Matrix Gla-protein: The calcification inhibitor in need of vitamin K
Quote:
The mechanism of vitamin K1 is believed to be most important for activation of hepatic clotting factors whereas K2 also is important for proteins synthesized in extra-hepatic tissues such as the vasculature...

...[the Rotterdam Study] demonstrated that dietary vitamin K2 intake (and not K1) was inversely correclated with cardiovascular calcification and cardiovascular death.

...[animal studies] found that K2 completely inhibited tissue calcification, whereas a similar or even an eight-fold higher dose of K1 had no measurable effect.

Vitamin K-dependent Proteins, Warfarin, and Vascular Calcification
Quote:
...although the liver seems to predominantly use plant-synthesized phylloquinones, vitamin K1, peripheral carboxylation is more dependent on the menaquinones, a structurally distinct group collectively known as vitamin K2.

Vitamin K2 supplementation prevents arterial calcification, yet vitamin K1 does not [in warfarin treated rats].

Vitamin K2 supplementation to those who require warfarin may provide a novel method to protect the vasculature while allowing anticoagulation.

So the answer to the question seems to be probably yes, with K2, and keep watch on the PT.

edit: Also, see here.


And thanks, Johnwen, for explaining atrial fib and prothrombin time so well!


Sun Nov 06, 2011 8:18 pm
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